Добірка наукової літератури з теми "D-lactic acidosis"

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Статті в журналах з теми "D-lactic acidosis"

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Petersen, Craig. "D-Lactic Acidosis." Nutrition in Clinical Practice 20, no. 6 (December 2005): 634–45. http://dx.doi.org/10.1177/0115426505020006634.

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2

Hayat, Muhammad S., Soon-IL Song, Zandra K. Ferrufino-Ponce, Nausheen Naz, and Frederick W. Ruymann. "D-Lactic Acidosis." American Journal of Gastroenterology 101 (September 2006): S377. http://dx.doi.org/10.14309/00000434-200609001-00947.

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3

Dunlop, Robert H., and Paul B. Hammond. "D-LACTIC ACIDOSIS OF RUMINANTS*†." Annals of the New York Academy of Sciences 119, no. 3 (December 16, 2006): 1109–32. http://dx.doi.org/10.1111/j.1749-6632.1965.tb47466.x.

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4

Lorenz, Ingrid. "d-Lactic acidosis in calves." Veterinary Journal 179, no. 2 (February 2009): 197–203. http://dx.doi.org/10.1016/j.tvjl.2007.08.028.

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Lorenz, I., and A. Lorch. "D-lactic acidosis in lambs." Veterinary Record 164, no. 6 (February 7, 2009): 174–75. http://dx.doi.org/10.1136/vr.164.6.174.

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6

Coronado, Boris E. "Antibiotic-Induced D-Lactic Acidosis." Annals of Internal Medicine 122, no. 11 (June 1, 1995): 839. http://dx.doi.org/10.7326/0003-4819-122-11-199506010-00005.

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Mack, David R. "D(—)–Lactic Acid Producing Probiotics, D(—)–Lactic Acidosis and Infants." Canadian Journal of Gastroenterology 18, no. 11 (2004): 671–75. http://dx.doi.org/10.1155/2004/342583.

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Анотація:
There is mounting evidence that ingestion of selected probiotics can modify disease morbidity for specific conditions affecting humans, and there is growing interest in the amelioration or prevention of disease with probiotics. Modulation in gene expression of the cellular elements of the intestinal mucosa and interbacterial interactions are leading theories as to the mechanism whereby probiotics can effect benefit for the host. Furthermore, gene-environmental interactions are considered to be important in the development of disease in those at genetic risk. With the intestinal tract harbouring large numbers of bacteria, alteration of the microbial environment with probiotic microbes is being considered as a controllable factor that may limit disease expression for those at genetic risk. This reasoning has led to interest in the administration of probiotics to infants. However, there are significant developmental changes occurring in many organ systems from the time of parturition and during the first months of life. Because there is little in the published scientific medical literature regarding the effects of long-term administration of probiotics to infants, potential problems must be considered; one such issue is that of administration of D(-)-lactate-producing probiotics. An appraisal of the current knowledge of this potential adverse effect is the subject of this communication.
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Bongaerts, G., J. Tolboom, T. Naber, J. Bakkeren, R. Severijnen, and H. Willems. "D-lactic acidemia and aciduria in pediatric and adult patients with short bowel syndrome." Clinical Chemistry 41, no. 1 (January 1, 1995): 107–10. http://dx.doi.org/10.1093/clinchem/41.1.107.

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Abstract D-Lactate produced by abundant intestinal lactobacilli during acidotic episodes in short bowel (SB) patients is commonly regarded as a main factor in the pathogenesis of SB syndrome-associated (D-lactic) acidosis. Since we had observed that gram-positive bacteria, mainly lactobacilli, were abundant even in the absence of acidosis, we studied serum concentrations and urinary excretions of D- and L-lactate in young and adult SB patients, especially during nonacidotic periods. Serum L-lactate and urinary L-lactate excretion were similar in adults and children. Serum D-lactate and urinary D-lactate excretion were higher in SB children than in SB adults. Food consumption affects D-lactate production and alters D-lactic acidemia and aciduria. We conclude that D-lactate is frequently present in serum of SB patients even in the absence of acidosis. High serum concentrations and urinary excretions may reflect dietary factors in these patients.
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Planas-Vilaseca, Alejandra, Fernando Guerrero-Pérez, Agustina P. Marengo, Rafael Lopez-Urdiales, and Núria Virgili-Casas. "D-lactic acidosis: A rare cause of metabolic acidosis." Endocrinología y Nutrición (English Edition) 63, no. 8 (October 2016): 433–34. http://dx.doi.org/10.1016/j.endoen.2016.09.009.

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Lorenz, Ingrid, and Arcangelo Gentile. "d-Lactic Acidosis in Neonatal Ruminants." Veterinary Clinics of North America: Food Animal Practice 30, no. 2 (July 2014): 317–31. http://dx.doi.org/10.1016/j.cvfa.2014.03.004.

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Дисертації з теми "D-lactic acidosis"

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Wallis, Amy. "Microbiota-Gut-Brain Interactions in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Focus on Neuropsychological Symptoms and Sex Comparisons." Thesis, 2017. https://vuir.vu.edu.au/37869/.

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Анотація:
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a chronic, disabling condition with debilitating fatigue and neuroimmune symptoms. Consensus about diagnosis, pathogenesis and efficacious treatments for ME/CFS are yet to be elucidated. Advances in the understanding of microbiota-gut-brain interactions in healthy and disease states, combined with evidence of gastrointestinal symptoms and gut dysbiosis in individuals with ME/CFS has directed investigation towards the role of enteric microbiota in this condition. The body of work presented in this thesis includes five publications based on reviews and empirical research conducted over the past 3.5 years. The first review paper (Paper 1) found preliminary evidence to support the proposal that microbiota-gut-brain interactions may contribute to sleep, mood and cognitive symptoms but revealed gaps in knowledge with few empirical studies that have investigated commensal microbiota in patients with ME/CFS. Papers 2 and 3 describe the results of a correlational analyses between microbiota and ME/CFS symptoms in a cross-sectional, retrospective study of 274 ME/CFS patients. A notable finding from this study included sex-specific interactions between gut microbiota and symptom expression in ME/CFS, signaling possible sex differences in microbial function. The systematic review examining symptom and etiological overlap between D-lactic acidosis and ME/CFS in Paper 4, revealed preliminary support for the hypothesis that subclinical concentrations of D-lactate from bacterial dysbiosis may be a mechanism contributing to several ME/CFS symptoms (including fatigue, neurocognitive impairments, pain, sleep disturbances, motor disturbances, gastrointestinal abnormalities, cardiovascular, respiratory, thermostatic, and comorbid mood and behavioural disturbances). The review highlighted the gaps in knowledge without measurement of D-lactate concentrations in ME/CFS samples. Paper 5 presents the results of an open-label, repeated-measures trial examining the efficacy of a 4-week treatment (alternate weeks of Erythromycin and D-lactate free probiotic) for an overgrowth of commensal Streptococcus species in 44 adult patients with ME/CFS. Large time effects were shown including a reduction in Streptococcus count and improvement on several clinical outcomes (sleep, cognition and total symptoms) for the total sample at post intervention. Ancillary results highlighted individual variability in microbial changes and the importance of other genera with changes in Bacteroides, Bifidobacteria and Clostridium and associated with clinical changes in males. In combination, the analysis of literature and results from both cross-sectional and experimental studies substantiate the theoretical premise that microbiota and gut dysbiosis contribute to specific neuropsychological symptoms in some ME/CFS patients. Our mechanistic understanding of gut dysbiosis will be advanced by multidisciplinary investigations that include assessment of clinical symptoms, the microbiome (combined sequencing and culture techniques), metabolites, oxidative and inflammatory markers, and immune profiles that help identify possible factors contributing to, precipitating or perpetuating imbalances in microbial composition. These advances may help clarify diagnostic discrepancies and inform efficacious treatment alternatives that are responsive to individual variability.
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Тези доповідей конференцій з теми "D-lactic acidosis"

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Kwasba, Ruth, Micheal Nwosu, Sunita Rajani, Zuzana Londt, Katie Green, and Arun Urs. "1275 D lactic acidosis – is it more prevalent condition than we think?" In Royal College of Paediatrics and Child Health, Abstracts of the RCPCH Conference–Online, 15 June 2021–17 June 2021. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2021. http://dx.doi.org/10.1136/archdischild-2021-rcpch.524.

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